Altered Sodium Channel Function Linked to Heart Failure

The results of a study, using mice and heart muscle cells from rabbits, by researchers from Georg-August-University Göttingen, Germany, have provided a potential molecular explanation for the abnormally rapid heartbeats known as ventricular tachyarrhythmias (VTs) that can cause the sudden death associated with heart failure.

Individuals who inherit mutations in genes regulating the influx of sodium ions (Na+) into the muscle cells of the heart through Na+ channels are predisposed to life-threatening VTs. So, because a protein known as calmodulin regulates Na+ channel function, and expression and activity of the calmodulin effector CaMKII is upregulated in humans with heart failure, Maier and colleagues investigated the effect of CaMKII on Na+ channel function. In this study, which appears online on November 22 in advance of publication in the December print issue of the Journal of Clinical Investigation, it was shown that overexpression of CaMKII in cultured heart muscle cells from rabbits and as a transgene in mice altered Na+ channel function. CaMKII mediated these effects by binding Na+ channel components and phosphorylating them. Importantly, mice overexpressing CaMKII were more susceptible to VTs than normal mice. These data lead the authors to suggest that CaMKII regulation of Na+ channel function might be a contributing factor to the onset of the potentially life-threatening VTs that are associated with heart failure.

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